Full Video – 19 minutes; Brief Video – 10 minutes

Unlike Zeus, or Athene, Janus did not come to Rome from Greece but from myths about a person living early in Roman history and later deified. Janus – deity – presides over beginnings and endings, gateways and doors, invariably dual in nature.

What is dual here?

Calcium stone formers are dual. A minority arise from systemic diseases we must screen for. Each systemic disease has its own universe of causes and treatment decisions. A majority are “idiopathic”, systemic causes have been excluded.

Idiopathic calcium stone formers are dual. They have no systemic cause of calcium stones. Most form calcium oxalate stones. A minority, more women than men, form calcium phosphate (CaP) stones.

Idiopathic calcium phosphate stone formers are dual. Most have hydroxyapatite (HA, like bone mineral) as their stone calcium phosphate. Some have brushite (Br, calcium monohydrogen phosphate) in their stones. These latter have more kidney damage than HA CaP stone formers, and are a special high risk group of patients.

Both kinds of CaP stone formers need special attention. That is why I have written this article for them.

Basic Facts about Phosphate Stone Formers

Phosphate Stones Damage Kidneys

Phosphate stones, HA or Br, can grow faster and larger than calcium oxalate ones. Calcium phosphate crystals invade kidney tissue – so called tubule plugs. Tissue damage is common, as is Nephrocalcinosis from plugging – often misdiagnosed as medullary sponge kidney. Kidney tissue damage is worse with Br than HA stones. Potassium citrate, a common stone prevention, may not be appropriate as a treatment because it raises urine pH.

Alkaline Urine Causes Phosphate Stones

Stone phosphate replaces oxalate when urine is too alkaline. Kidney and GI tract physiology raise urine pH, especially in women. Diet is not the cause of higher urine pH. Diet will not reliably lower the pH, and we have no specific drugs to do it, either. So although treatment uses the same tactics as for the more common calcium oxalate patient, it must follow a different strategy.

How Stone Analysis Distinguishes CaP from CaOx Stone Formers

Only CaOx and HA Present

If the average stone mineral composition of all available stones for a given patient is above 50% calcium oxalate, the patient is considered a calcium oxalate (CaOx) stone former. If the average calcium phosphate content is above 50% the patient is considered a calcium phosphate stone former.

The average must be computed using 0 – for example, given CaOx/CaP percentages of 100/0, 0/100, 40/60, the correct classification is 140/3 vs 160/3 or 46% CaOx vs 53%, and so a CaP stone former.

Uric Acid, Struvite, Cystine Also Present

If uric acid, struvite, or cystine are present we name the patient for that constituent. A patient who forms mixed stones – for example, 60% calcium phosphate/20% struvite 20% CaOx is called a struvite stone former. The reason is that these stone types have special causes and treatments. 

Any Brushite Present

Brushite is very uncommon in human kidney stones, and associates with large tubule plugs and more severe tissue damage. So when any stone contains brushite we classify the patient as a brushite stone former even though brushite is a minority of stone mineral.

Sex and Age

Single Clinic Experience

Percentages of Cases

CaptureThe table shows ‘CaP’ as cases where HA or brushite was the stone phosphate crystal (in early years we did not distinguish). CaP(b) are CaP stone formers with only HA, no brushite in any stone.

CaP predominate among females (a and b superscripts denote outsize high frequencies). Brushite does not show this difference a statistical level of significance. CaOx stone formers predominate among the total of all cases. Brushite patients are least common.

Sex vs. Percent CaP in Stones

The same study furnished this nice graph showing the sexes as the percent of stone CaP increases. The bulk of patients have very little CaP in stones (tall bars at the left of the graph). These are the common CaOx stone formers, mainly men (% female, dots, right axis about 25%). But when CaP percent is 20 – 50% in stones, women and men are nearly equal.Capture 2

This graph blurs the sex distinction because we used stone CaP% from both brushite and hydroxyapatite. Today, I would have left the brushite to one side, which would have made the female preponderance among those with high stone CaP% more marked – because the sex ratio for brushite stone formers is closer to 1.

National Laboratory Findings

The Mayo Clinic kidney stone analysis laboratory analyzed 48,446 stones in 2010, and of these 43,545 were the first submitted to the lab for that person. From these stones, they report the distribution of stone type by sex and age. I have made a graph from Table 2 of their publication.

Population Sex Ratio

stone rates and male to female stone and population ratios from Lieske

The general population contains more males than females at younger ages (blue dots). By age 30-39 the two sexes are present in equal numbers. Thereafter, as men predecease women, their blue dots slump downward.

For all ages combined, the ratio of men to women is just under 1 (last blue dot at right).

Stone Former Sex Ratio

The blue bars show male to female ratios among stone formers. Remember this is counted from the sex of the person whose stone was analyzed. A survey based on symptomatic rates of stone passage, by contrast, might give different results altogether.

In childhood, men have slightly more stones than women (blue bar is above 1.0). In the teen years and up to age 39, women predominate over men (blue bars are below 1.0). After age 40 men predominate, until at age 90 and more, in this and perhaps most things, the sexes come into a near perfect alignment. Averaged over all of life, men have more stones, which appears to be because of their midlife excesses (Height of the ‘ALL AGES’ bar above 1.0).

The fraction of all stones formed (red dots; scale along the right axis) for both sexes combined is highest from age 20-69, with only a small fraction in childhood or old age.

Types of Stones

sex and age vs stone type from lieske

The men are on top, women on the bottom of the picture to the left.

Stones were classified using the system I have used on this site. Uric acid in any amount meant the stones were classified as uric acid stones, and likewise for any struvite or cystine.

CaOx stones preponderate among both sexes over all ages, except in women between ages 20 – 39 stones were about half CaOx and HA. With age, HA stone frequency fell in both sexes, so that most men, and most older women (over 40) have CaOx stones.

Brushite stones, in both sexes, are very uncommon. You can see them as triangles along the bottom of both graphs.

Over age 50, uric acid stones become a significant concern in both sexes.

Struvite stones, which always arise from infection with bacteria that possess urease, are more common in women than men, a fact known for ages.

The Mystery of Brushite

Brushite stones are rare but should be rarer still. I have written a whole article on brushite because it is so important and yet so evanescent. It forms first of all crystals in human urine. If pH is not too high, oxalate steals away its calcium atoms so it vanishes. If pH is high, HA does the same, and brushite vanishes.

Why, then, are there any brushite stone formers?

I do not know nor does anyone I know of. It is an open question that seems obscure but whose answer might well lead to some new understanding of how stones form.

The Importance of Brushite

Being the first crystal to form, brushite supersaturation is crucial for stone prevention, a fact not intuitive but worthy of special emphasis. Rare in stones, vanishing in most urine, yet brushite supersaturation is foremost in importance for clinicians and patients. The goal is a supersaturation below 1, so brushite cannot form. For those who want to know more about why, please look at the parent article.

Time and Shock Wave Lithotripsy

We (left hand figure below) and others have noted an increasing percent of CaP in stones over the past 30 years. In women (black dots) CaP percent is always higher than in men, but it has risen in both. For those of a quantitative bent, the time trend of stone CaP tested by ANOVA with post hoc contrasts was significant for both sexes, and women were higher than men throughout.

In the publication, we found a relationship between CaP cappercent vs decades from parks phosphate paperpercentage and numbers of shock wave lithotripsy procedures. Use of potassium citrate, however, did not seem to increase stone CaP.

The number of shock wave procedures per patient adjusted for the number of stones and the years of stone disease rose with the percent of CaP in stones (Panel A of the figure below to the right) and the percent of CaP likewise adjusted for number of stones and duration of stones and sex rose progressively with the number of shock wave procedures (Panel B of figure to the lower right).

Not shown here, but of interest, the number of shock wave treatments was higher among BRSF than HASF suggesting a link between shock wave treatment and brushite stones.

One might infer from this set of graphs that the advent of shock wave lithotripsy caused the increase in phosphate stones, and there is nothing to contradict the idea. In fact, the very physiology of phosphate stone formation and the effects of shock waves on kidney swl and stone capfunction strongly support that idea as I shall show you.

Mechanisms of Phosphate Stone Formation

High Urine pH

As expected, percent CaP in stones (upper left panel of the figure below) rises with CaP SS. I have shown elsewhere on this site that stone crystals parallel urine supersaturations.

Because CaP SS depends powerfully on urine pH one expects and finds (upper middle panel) that urine pH tracks very closely with stone CaP percent. Urine calcium, volume, phosphate, and citrate excretions (remaining panels) had no important relationship to stone CaP percent. 

But take a look at the urine calcium excretions (Upper right panel). They are very high on average. This is because a high fraction of all calcium stone formers have genetic (idiopathic) hypercalciuria. Risk for stone forming begins at a urine calcium of 200 mg/d in both sexes.

determinants of phosphate stones sixplot

So you can think of CaP stones as a two hit model.

Genetic hypercalciuria promotes calcium stones, and urine pH controls the fraction of phosphate in the stones. High CaP SS and CaP stones require a urine pH significantly above 6 as shown in the upper middle panel.

Kidney Tissue

Plaque and Plugs

CaOx stones can be produced as overgrowths in interstitial HA deposits, called plaque.

Idiopathic CaP stone formers, and patients with stones from bowel disease, ileostomy, renal tubular acidosis, and primary hyperparathyroidism, form stones on plaque but also on plugs of HA that fill and damage the last millimeter or so of the nephron, the inner medullary collecting ducts and ducts of Bellini.

Although we are not certain, I think it is fair to say that the plugging of CaP stone formers is because more CaP crystals form in urine and can produce plugging. In a recent article I trace out how calcium phosphate actually forms, how it is a rapid process compared to calcium oxalate, and therefore more able to make plugs during the short times it takes for urine to pass out of tubules into the renal pelvis.

Distinctions Among the Three Idiopathic Calcium Stone Formers

We have table from ha br caox comparison paperpublished selected laboratory and tissue findings of CaOx, brushite and HA stone formers, in an attempt to clarify differences in how stones form, and amounts of tissue injury.

Numbers are small because each patient had been studied with intra-operative imaging of the renal papillae and papillary biopsy: 11 CaP (HASF), 25 BR (BRSF), and 30 CaOx (ICSF) stone formers.

As expected, urine pH was higher in the BRSF and HASF than in the ICSF, as was supersaturation (SS) for CaP. Incidentally, urine calcium (Ca) was also higher in both CaP groups than in the ICSF.

Mainly CaOx and BR stone formers formed plaque, and mainly CaOx SF form stones on it. About 8% and 6% of papillary surfaces were covered with plaque in ICSF and BRSF but only 0.8% among the HASF. CaOx stone formers had an average of 10 stones/patient attached to plaque, vs. only 3 plaque stones in 25 BRSF and 6 in 11 HASF stone patients: 10/ CaOx patient  vs 0.12/brushite patient and 0.54/HA patient. These are 80 and 18 fold differences, respectively!

Plugging (‘deposits’ in the table) was absent in ICSF, but common in BRSF and HASF. Plug size averaged 1.6 mm2 in BSRF but only 0.4 mm2 in HASF – a 4 fold difference. The number of plugs was 3 times higher in HA vs. Br patients: 12 vs. 3/mm3 of tissue volume. BRSF formed fewer but much bigger tubule plugs.

Calyx dilation (a abnormal finding) estimated during surgery was higher in HASF than in the other two groups, and papillary injury (papillae are the parts of kidneys inside calyces) higher in both phosphate groups than in ICSF.

In the kidney cortex, far from where stones form, many CaP stone formers had scarring (TIF, tubular interstitial fibrosis) vs. very few CaOx patients. Brushite patients had most cortical damage.

So phosphate stone formers have injury involving the papillae and cortex, whereas CaOx stone formers have almost none.

Why is Urine pH High?

Being Female

I wrote a whole article on how women raise their urine pHThey do it by absorbing from their food a higher fraction of its alkali content. No sense copying all that here, it is better to read the article. High GI alkali absorption is not easy to treat. Those alkali are nutrient – anions that cells metabolize to get energy. 

Being Young

We used a massive database of kidney stone formers to ask what happened to urine pH in men and women with age. The answer is it falls, in both sexes (women are circles, men triangles).

Why is a long story. We could exclude gain in BMI, loss of kidney function, and GI alkali as reasons, but could not find the reason itself. In fact, GI anion absorption rose with age, as if to offset the falling pH.

Here the important fact is on the graph – higher pH in women and in youth are an obvious cause of more CaP stones.

Shock Wave Lithotripsy (SWL)

No practical experiments permit us to measure effects of SWL on urine pH in humans.

For these reasons we turned to an animal model: The farm pig whose kidney is much like that of a human, and likewise is similar in size.

In these animals we could shock one kidney, and then compare the treated to control side at time intervals after the treatment, the untreated side being a perfect control as both kidneys are bathed by the same blood.

SWL Raised Urine pH.

Urine pH from the treated kidneys was 0.18 pH units higher than the control, meaning SWL had increased urine pH (first line of table under ‘Basal’).

SWL Damaged Kidney Tubule Function

There was a lot more.

Urine flow, and excretion of bicarbonate, potassium, chloride, sulfate, calcium, magnesium, sodium and oxalate all were higher from the treated side (bolded). This means that shock wave treatment affects tubule handling of multiple molecules, presumably because of injury.

table 2 from swl paperWe could find these abnormalities up to 90 days after shock wave. The control kidney reduced its losses in compensation so blood remained entirely normal.

Bicarbonate Losing Raised the pH

The higher urine pH could have been due to damage of final urine acidification in the collecting ducts or to high delivery of bicarbonate from higher up in the nephron so that acid secreted lower down was neutralized by a flood of bicarbonate.

To tell these apart we gave the pigs an acid load that lowered their blood bicarbonate and therefore filtration and downstream delivery (‘Acid load’ columns). Acid load brought urine pH and almost all other measurements to equality between the shocked and control kidneys (loss of bolding).

The tissues from the pigs showed widespread injury to the thick ascending limbs, and you can read the paper for details.

SWL Can Raise Urine pH by Damaging Kidney Tubules

The meaning of the work is clear.

After shock wave treatments the treated kidney may excrete excess calcium and produce a urine of higher pH than it would otherwise do. The effects are precisely those needed to produce calcium phosphate crystals. From the bladder urine, which mixes urine from both kidneys, one could never know this was happening.

It is possible that the advent of shockwave lithotripsy has contributed to the rise in CaP stones, and I hope that further science sorts out whether this hypothesis is false or true.

High Kidney Ammonia Production

Ammonia Production Regulates Urine pH

Kidneys excrete acid by making ammonia that can carry acid (protons) into urine without lowering urine pH. They also excrete acid by titrating urine phosphate, which does lower urine pH. If ammonia production goes down, from kidney disease, for example, urine pH has to fall so acid can be lost on phosphate.

Ammonia production relates itself to body acid load – from food and metabolism – so that the average urine pH is just around 6. But what would happen if regulation were abnormal so more ammonia than normal was made for a given bodily acid load?

Urine pH would rise.

CaP Stone Formers Make More Ammonia

The graph shows urine ammonia excretion from normals, and CaOx and CaP stone formers studied eating the exact same diet in a research center.

Fasting, all three groups are the same (left panels). Food increased urine ammonia in male CaP patients (#). Fed, the female CaP stone formers produce more ammonia than female normals (*, top right panel). So do the female CaOx stone formers. Ammonia production is governed by body acid load, which we measure as GI anion and urine sulfate – a residue of metabolic acid production. When we adjust ammonia for acid load (lower right panel) CaP stone male and female stone formers remain high compared to same sex normals.

We suspect the high urine pH that causes CaP stones arises in part from high ammonia production, perhaps an inherited trait.

Low Urine Citrate

Many articles on this site explore the powerful effects of citrate to bind calcium and inhibit calcium crystal growthIn these closely 

studied men and women we could document a uniquely low urine citrate of CaP stone formers vs. normal people.

Low Citrate in CaP Stone Formers

Food increased urine citrate is normal women and all three male groups (#). With food, CaP stone formers of both sexes have urine citrate excretions below their same sex normal counterparts (*, upper right panel) as did female CaOx stone formers.

As is well known, citrate is lower in normal men than women (compare black bars; we did not choose to compare the sexes statistically).

Adjusted for GI alkali and urine sulfate, (lower right panel) low citrate is concentrated among male CaP and female CaOx stone formers. Normal men remain below normal women.

Male CaOx stone formers have abnormally high urine citrate with and without adjustment for systemic acid balance.

Abnormal Kidney Cell Citrate Handling

Alkali loads, most famously potassium citrate, raise urine citrate and is an established stone preventionCitrate also raises urine pH, because the alkali appears in urine as bicarbonate. That is why potassium citrate is not an ideal treatment against CaP stones, and why we have for decades needed a controlled trial to see if it works or makes things worse.

But here we have a high urine pH coupled with low urine citrate, in male CaP and female CaOx and CaP stone formers. That points to something wrong with kidney cell regulation.

We measured serum citrate and glomerular filtration so we could calculate the fraction of filtered citrate excreted (FE Citrate), shown in the upper right panel of the graph at left.

FE citrate is low in female CaOx and CaP stone formers and in males with CaP stones. This means that CaP stone formers are reabsorbing abnormal amounts of citrate back from the filtrate. It is used by kidney cells to produce metabolic energy.

Adjusting for GI alkali absorption (lower right panel) removes the female abnormalities but makes the male one even more prominent.

That male CaOx stone formers have abnormally high urine citrate excretion with normal FE citrate is because their serum citrate concentration is higher, a fact for which we had no explanation.

CaP Stone Formers Have Proximal Tubule Abnormalities

Citrate reabsorption and ammonia production are linked in the proximal tubules of the kidneys as part of overall kidney regulation of bodily acid base balance. In general alkali loads raise urine pH and urine citrate, and reduce ammonia production, whereas acid loads do the opposite.

Here we have high pH and high ammonia production coupled with low urine citrate, more marked in male CaP patients but detectable among the women as well.

It is as though the cells perceive a need to produce more acid excretion (ammonia) and conserve potential alkali (citrate is metabolized to bicarbonate), but there is no need. So urine pH rises and converts calcium stones to their phosphate forms. The cause(s) of these proximal tubule abnormalities are not known.

Incomplete Distal Renal Tubular Acidosis (dRTA)

A Questionable Disorder

Some have proposed that CaP stone formers have high urine pH and low citrate as part of “Incomplete renal tubular acidosis”. In proof, when given extra acid they may not reduce urine pH as low as normal people. In my primary article on dRTA, I present contemporary evidence that acid loading creates a continuous spectrum of urine pH responses, even among normal controls, so it is not a good basis for diagnosis. It seems better to say that CaP stone formers have abnormal proximal tubule functions, and make those the focus of new science.

Heterozygotes of Familial dRTA

With one exception, hereditary dRTA arises from gene disorders of the main proton transporters or of carbonic anhydrase itself, and these disorders are in general recessive. They are recessive because you need two defective genes to knock out a transporter whereas one good gene copy will maintain function.

Of course dRTA causes massive CaP stones and kidney disease. But heterozygotes – meaning one good and one defective gene – from families with dRTA if studied in detail, may not lower urine pH normally. These might be diagnosed as ‘incomplete dRTA, because in fact that is what they are.

CaP Stone Formers are Not Like Incomplete dRTA

Unlike our CaP stone formers, urine ammonia is low in dRTA and heterozygotes from families of dRTA, when compared to their acid load – urine sulfate. Urine ammonia is never high. I suspect that some CaP stone formers have high urine pH because they are indeed heterozygotes of dRTA. Low ammonia may be a way to separate them from the high ammonia of routine CaP stone formers.

Risk of Conversion From CaOx to CaP Stones

Some patients gradually increase their stone CaP percent, often enough to alter their classification to CaP stone former. The opposite, conversion from CaP to CaOx stones must be very uncommon, as we have no cases to report. We wanted to know how to detect risk of conversion.

Who We Studied

From 4767 patients in our program, we collected all CaOx stone formers who had two or more stone analyses and clinical follow up data (445 patients). From these we selected all who had a last stone CaP% at least 20% higher than that of the first stone (62 patients). Men and women were combined because we had so few cases.

Of these 62 cases, 26 had had three initial (pre-treatment) 24 hour urine studies before they passed the stone whose CaP percent was at least 20% higher than their first stone. We labeled these transformers with prior laboratory work – labs before they transformed – as ‘TP’.

the 26 converting patients with pre conversion labs TC group

For controls we chose 181 patients whose first stones were >90% CaOx and who increased their stone CaP percent <20% between the first and last stone.

This figure shows the 26 TP cases and the 181 controls.

CaP% Was High at the beginning

Even though their initial stone CaOx percent was >50%, the 26 TP cases (black circles, upper left panel) had an average stone CaP of 10% before treatment, whereas it was much lower in the controls – who never added significant CaP.

During follow-up (upper left and middle panels) the 26 TP (black circles) increased their stone CaP markedly (average 10% to 79%, top left). The controls (gray triangles) hardly changed (-0.6% for controls, 69% change, for TP, upper middle panel).

Higher Urine pH Increased CaP SS

Urine pH and CaP SS before treatment and before conversion (upper right panel and lower left panels) and during treatment (lower middle and lower right panels) were higher in TP (black circles) than controls. CaP SS rose because we used potassium citrate as part of our treatment program.

SWL May Have Played a Role

ESWL associated with conversion: 112 of the 136 total cases with no ESWL procedures were controls, whereas only 21/41 cases with >2 ESWL were controls (X2=17, p<0.001). Furthermore, a predominance of ESWL procedures preceded the final stone (not shown here but shown in the paper), meaning ESWL could have been a causal factor.

Who is at Risk?

When stone CaP is above 10%, average 24 hour pH is as high as 6.3, or CaP supersaturation is above 2 before treatment risk of increasing stone CaP may be high. More than 2 ESWL procedures likewise. Given these risk factors in a CaOx SF perhaps one is prudent to treat as if CaP stones were already forming, so as to possibly prevent further stone CaP accumulation.

Prevention of Calcium Phosphate Stones

The objective is to lower CaP SS – reported with respect to brushite – below 1.

The main modifiable factors are urine volume, and calcium and citrate excretion. Because we cannot lower urine pH, the most crucial factor, we have to use what is left to achieve our goal. Likewise, because citrate regulation is abnormal in CaP stone formers, use of potassium citrate may not raise urine citrate so much as it raises urine pH, and therefore this otherwise valuable treatment can be ineffective.


Relative calcium stone risk falls to 1 (no excess risk) at about 2.3 l/d of urine volume. Given the limitations of our treatments, I usually strive for 2.5 l/d spread out over the waking hours. This is an achievable goal if patients understand why it is important for their stone prevention.

Reduced Calcium Excretion

Genetic hypercalciuria is very common among calcium stone formers. If we understand that relative risk of stones rises above 1 at a urine calcium of 200 mg/d, both sexes, our goal is to reduce urine calcium to or below that point.

Reduced Diet Sodium

Multiple articles on this site detail the power of diet sodium to control urine calcium and bone calcium balance. The US diet recommendations for sodium are 100 mEq (2300 mg)/day as a tolerable upper limit, and 65 mEq (1500 mg)/day as ideal. These values concern blood pressure and bone rather than kidney stones. But if we achieve an ideal diet sodium it will lower urine calcium as well as defend blood pressure and bone mineral. So I have no reservations about promoting the ideal diet sodium, but also am prepared for compromise in this fast food dominated world.

Reduced Diet Sugar

As for diet sodium, I have written extensively about sugar as a factor that raises urine calcium, abruptly after the sugar load and with proven increase in supersaturations. Once again, US guidelines call for reducing sugar intake, and there is no benefit to anyone from eating refined sugar in any form. So I am shameless in my zeal to encourage patients to eat as little of it as possible.


Drugs of this class lower urine calcium about 80 to 100 mg/d below the level predicted by sodium intake. They act in part to increase proximal tubule calcium reabsorption. They are trial proven agents to reduce calcium stone recurrence. We have shown thiazide drugs lower urine pH, a possible benefit.

I have often argued to use diet as much as possible before adding thiazide to avoid drug side effects. But phosphate stones are not easy to prevent, so far as I have observed, and they damage kidney tissue. Moreover, we have no trials – none. These patients may have been in trials but are doomed to perpetual minority status unless specifically a focus.

So I am not shy about adding thiazide after perhaps only one to two efforts at diet control, should CaP supersaturation remain above 1.

Why NIH has yet to fund a calcium phosphate stone prevention trial escapes me. I cannot imagine how this has not been a priority.

Potassium Citrate  

This drug will lower urine calcium below the level predicted by diet sodium intake. It may raise urine citrate excretion. But It may also raise urine pH.

Being as it is therefore able to raise or lower CaP supersaturation, I do not so much avoid using it as view it with a cold eye.

If thiazide is not attractive to a given patient I will try citrate and watch the effect on CaP supersaturation. CaP supersaturation is the final resultant of whatever changes it induces in urine calcium, pH, and citrate. If it indeed lowers CaP supersaturation, I am prone to use it but with appropriate 24 hour urine followup and an inextinguishable skepticism.

Reduced Diet Oxalate

I am aware that calcium oxalate in stones matters, and that even high phosphate stones often contain that crystal. If urine oxalate is high enough to confer risk – above 25 mg/d in both sexes – I make appropriate diet recommendations.

But patients cannot do everything all at once, so I generally put most emphasis on the calcium phosphate side. The exception is when urine oxalate is quite high – above 40 mg/d, for me – whereupon I do what I can with diet.

Monitoring Treatment

The objective is to lower CaP supersaturation below 1 in the 24 hour urine, and that is what I aim to achieve.

If fluids are enough, so be it. If not I add more treatments more or less as in the paragraphs above. Lacking trials, this is the best we can do. I watch supersaturation for calcium oxalate as a secondary endpoint, and if it is high enough to promote risk – above 3 – I attempt to lower it by reducing diet oxalate.

Monitoring is crucial. What we try to do may not be done because patients cannot or will not do it, so we have to know when to try another approach.

Put another way, for stone prevention, especially calcium phosphate stones, deliberation is reality.

I wish to thank Dr John Asplin for his careful reading of this article and suggestions for improvement. 



78 Responses to “CALCIUM PHOSPHATE STONES: Causes and Prevention”

  1. Traci

    I have had four stones all large requiring surgical intervention. The earlier ones were calcium oxilate and the last 1.2 cm stones was 100% brushite. My urine calcium is 350, urine volume 2.7 liters, citrate 400, SSCap is 2.1, PH 6.8. I am wondering what I should be on: 1. Chlorthalidone 12.5mg/day and try to not supplement with potassium citrate since my super saturation of calcium phosphate and PH are rather high. However, it will not reduce calcium as much or 2. High dose of chlorthalidone at 25mg a day plus potassium citrate (since my potassium will surely go down).

    • Fredric L Coe

      Hi Traci, Brushite stones are always a problem, often large, numerous, and hard to disrupt with with lasers or shock waves. The treatment approach to your high urine calcium begins with sodium, which often solves the problems you mention. You want to lower diet sodium to below 1500 mg/d if you can, and see how far down that takes your urine calcium. Then you add chlorthalidone on to the diet in the lowest dose that is workable. Here is a good review of the process of combining diet with meds effectively. Regards, Fred Coe

  2. Waheeda Samji

    I’m 34 yr old female and had my first kidney stone with a 97%CaP content

    Waiting for the urinalysis

    And I have no other symptoms – where can I find details about high % stone formation?

    • Fredric L Coe

      Hi Waheeda, This article speaks precisely about you. Evaluation and treatment are in the article and very important for you to follow. Regards, Fred Coe

  3. Lanie Allen

    Hi, had several small stones removed with Lithotripsy, then 16 months later had enormous stone form … 27 mm in same kidney, it is calcium phosphate. I agree with your findings.

    • Fredric L Coe

      Hi Lanie, Be sure you have full evaluation for cause with 24 hour urine and blood testing and go on a proper regimen for protection against more stones. Phosphate stones can form and grow rapidly and are often caused by high urine calcium and pH. The former is not hard to treat, the latter is not directly treatable. Regards, Fred Coe

  4. Nichole

    These articles are so very helpful. I am a 35 year old female with 15+ years kidney complications, urethral pain, flank pain, stones, and hematuria (consistent 2015-present) without identifiable cause. CKD Stage 3 at 50 GFR diagnosed at age 28 that I managed to improve now testing between 60-78 GFR the past year. Age 27 diagnosed with Dysautonomia including Chronic Migraine, Sensory Disturbances, Postural Orthostatic Tachycardia Syndrome and Suspected Mast Cell Activation Syndrome (MCAS). MCAS presentation includes falres of wide spread itching skin rash inconsistent with urticaria pigmentosa, bilateral eye watering, swelling, abdominal distention, GERD/SERD, Elevated PGF2a and cyclic vomiting. Cystocopy unremarkable, Endoscopy and Colonoscopy biopsy revelaled borderline (20-25 Mast Cells per/HPF) Hiatal Hernia, otherwise unremarkable. Highly sensitive to most medications and food additives but no identifiable allergy.
    There is speculation kidney disease is an underlying condition leading to Autonomic Dysfunction/Dysautonomia and MCAS symptoms closely resemble symptoms of poor kidney filtration. Family history of Lupus and X-Linked Alport Syndrome (Confirmed I do not have the Alports mutation)

    Below are my 24-Hr results which I notice are elevated for Brushite but I’ve not found the reference level in my results on the graphs provided in the articles I’ve read so far and am not sure what to make of this information. Unfortunately I cannot see Nephrology until September. To note the say after providing my 24-hr urine sample I broke out in widespread spots 3″ x 3″ +/- itchy and felt as though my entire body was sunburned. Very curious if Brushite or it’s cause may also explain the bigger picture:

    Component Your value Standard range
    SPECIMEN VOLUME 24 HR URINE 1.15 L/day >2.00 L/day
    PH, 24HR URINE 6.7 5.5 – 7.0
    CALCIUM RATE, 24 HR URINE 510 mg/day <250 mg/day
    OXALATE RATE, 24 HR URINE 25 mg/day <45 mg/day
    URIC ACID RATE, 24 HR URINE 726 mg/day 320 mg/day
    SODIUM RATE, 24 HR URINE 188 mEq/day <200 mEq/day
    PHOSPHATE RATE, 24 HR URINE 867 mg/day 60 mg/day
    24HR URINE AMMONIA RATE (UMOL/24HR) 24 mEq/day 14 – 62 mEq/day
    POTASSIUM, 24 HR URINE 50 mEq/day 19 – 135 mEq/day
    CREATININE RATE, 24 HR URINE 1479 mg/day 600 – 1800 mg/day
    C3 173 mg/dL 90 – 180 mg/dL
    C4 36 mg/dL 10 – 40 mg/dL
    PROTEIN, URINE, QN 10 mg/dL <=11 mg/dL
    CREATININE, URINE 131 mg/dL mg/dL
    GLUCOSE, UA <30 (Neg) mg/dL Negative mg/dL
    KETONES, UA <10 (Neg) mg/dL Negative mg/dL
    SPECIFIC GRAVITY, UA 1.015 1.005 – 1.030
    UA HGB 1.00 (3+) mg/dL Hb Negative mg/dL Hb
    PH, UA 6.5 5.0 – 8.0
    PROTEIN, UA <10 (Neg) mg/dL <30 (1+) mg/dL
    NITRITE, UA Negative Negative
    LEUKOCYTE ESTERASE, UA Negative Negative
    UROBILINOGEN, UA, QL 0.2 (Neg) mg/dL Negative mg/dL
    BILIRUBIN, UA <0.5 (Neg) mg/dL Negative mg/dL

    • Fredric L Coe

      Hi Nichole, Your stones surely arise from the extremely high urine calcium level of 510 mg/day. The urine is alkaline with pH of 6.7 and that is why your stones are brushite – calcium monohydrogen phosphate. You have a very high sodium intake of 188 mEq/d and scanty urine volume of 1.15 liter/day. So you need treatment aimed at much higher urine volume, low diet sodium, and probably a medication to lower urine calcium. Here is a good article close to what you have. I urge you speak with your physicians about the possibility of pursuing treatment as prevention seems obvious and very likely. Regards, Fred Coe

  5. Gerald

    I had a GSW to abdomen with a partial whipple, partial R Nephrectomy, and had some small intestine removed. I actually have hypoparathyroidism; just under the low mark by several points. I have had kidney stones for over 20years and am now suffering CKD. Creatine 1.5 and GFR fluctuates in the 50’s. I am 48. I need a really good doctor to help me figure this out. So far, all I can manage to get from my doctors, and I have seen many, is the same thing…treat me then send me home. My stones have gradually increased from Calcium Oxalate to 50/50 oxalate/phosphate. I am in Florida near Tampa. I have many stones in the kidneys and they are difficult to treat. Horseshoe kidney makes things a bit more complicated; at least for some doctors. I even had one send me home with a referral from ER when I had a complete obstruction with a rising creatine. He didn’t want to touch me. I am at a loss and very frustrated. I would even travel to Chicago or anywhere to receive the right treatment.
    Many thanks,

    • Fredric L Coe

      Hi Gerald, You indeed have a very complex problem. I know of no facilities in Tampa, but there is a fine kidney stone group at the university in Gainesville. Chicago seems harder to get to but if you wish to come up here we can arrange for the consultation you need. Let me know what would be easiest for you. Regards, Fred Coe

      • Gerald DuBois

        I am going to have another 24hr urine and all relevant bloodwork done; as well as a ct. May I send the results to you. Perhaps I can arrange with your office for a consult. Having had the opportunity to see the results of the tests and records, I am hoping you can shed some light on this. I am scheduling soon to have my kidney stones dusted and kidneys cleaned out. I just do not want to do so and not have a clear plan for future prevention. I have to save my kidney function

        • Fredric L Coe

          Hi Gerald, Medicine is a very complicated space. On a site like this I can offer information, even up to specific ideas for patients to think about and bring to their physicians. But if it comes to a review of medical records and tests for the purpose of practicing medicine, that is structured. Presently, my institution permits me to provide care for patients who come to see me. Telemedicine is not as yet available as a member of the UC medical staff and as a professor of medicine. If your physician wants me to review your records and report to him/her about my opinion, we can arrange that. Of course you would receive whatever is sent. Absent our meeting I cannot review your records and tell you how I think you need to be treated, that is improper practice of medicine. Please let me know what you might like within this framework. Regards, Fred Coe

          • Gerald DuBois

            I would gladly make an office visit with you if you can provide whom to contact.

            • Fredric L Coe

              Hi Gerald, That is the easiest way to do it. My secretary is Karen Niswander, 773 702 1475. She can make all arrangements. Regards, Fred Coe

  6. Brenda OBrien

    Hi Dr. Coe,
    I am a 60 year old female who has been having kidney stones for the last 10 years. My medication list is as follows: flecainide for A-fib.,
    gabapentin for neuropathy,
    cholestyramine for irritable bowel syndrome,
    fosamax, along with a calcium supplement and vitamin D for osteoporosis.
    My blood work is all in the normal range.
    The results from my 24 hour urine test are as follows:
    calcium oxalate urine-: 1.52 Delta G
    Calcium Hydrogen Phosphate dihydrate: 0.34 Delta G
    Hydroxyapatite : 6.15 Delta G
    Urate Urine: -5.14 Delta G
    Sodium Urate: 0.10 Delta G
    Sodium: 103 mmol
    Potassium: 27 mmol
    Calcium:189 mg
    Magnesium: 63 mg
    Chloride: 76 mmol
    Phosphate: 399 mg
    Sulfate: 8 mmol
    Citrate: 611 mg
    Oxalate: 0.23 mmol
    ph urine: 6.8
    uric acid: 378 mg
    creatinine: 1050 mg
    Osmolality: 218 mOsm/kg
    Ammonium: 25 mmol
    urea nitrogen: 4.9 g
    protein catabolic rate: 56 g
    My urologist has told me to drink 2 quarts of lemonade a day, increase fluids and eat a low sodium diet, which I have been doing , but I am still getting stones. I was wondering if you had other ideas of what I can do to aide in the prevention of these stones.
    Thanks so much for your time,

    • Fredric L Coe

      Hi Brenda, You do not mention the type of stone but the high pH suggests calcium phosphate. Your urine has some odd features in that your sulfate is low compared to your urine ammonia, this suggests potassium depletion, or some odd diet patterns. You do not mention the volume of the 24 hour urine, was it in fact 2 liters as you suggest? With a lot of gaps, I cannot be much help, but perhaps you could fill in the volume and stone type. Regards, Fred Coe

  7. Katie

    Hi! thank-you for all the amazing information! I have been passing kidney stones for the past 15 years. For a long time it was just 1 every couple years, but in the past couple years it has been picking up pace. Now it is at the point where I am passing them monthly. I passed 2 already this month and have another stubborn one trying to pass now again already. I just turned in the 2 I passed this month and got my results today: 40% calcium phosphate (apatite), 30% calcium oxalate monohydrate, and 30% calcium oxalate dihydrate. Waiting for results from my 24 hour urine collection still but my blood work they took when i turned in my stones this week looked normal.
    Potassium, S 4.1 mmol/L
    Chloride, S 99 mmol/L
    Calcium 9.1 mg/dL
    Sodium, S 140 mmol/L
    Bicarbonate, S 26 mmol/L
    Anion Gap 15

    Any input from this info while I am impatiently awaiting my appointment with the specialist? I had a couple tiny blood clots in my urine this month too which I have never seen before. Is this something you have seen before? and everytime I end up in the ER I have very low elevated WBC count which they bring up every time but it seems too low for infection. And last of all, I was curious if any of these kidney disorders you have mentioned had the symptom of a face rash? maybe its not related but it is another weird symptom i have been getting the past months too. it is a defined red rash on cheeks and nose and sometimes goes up on forehead and it burns! It comes on suddenly for an hour or so and then disappears. Again maybe not related but just with the increase in urinary/kidney issues I was thinking maybe it was all tied together. I live in a smaller town and we don’t have the best doctors all the time so it is all making me nervous. Any input would be appreciated. Thank-you!

    • Katie

      Ok now got my 24hr urine results back and they seemed really bad. i dont get why they are so off but my blood levels are normal. For example my urine calcium was over 500! Also elevated was my Chloride (314 mg), Uric Acid (1200 mg), Creatinine (2415 mg), Urea Nitrogen (21.4 g), Sodium (282 mg), Potassium (84 mg), protein catabolic rate (159 g). and Ammonium (only by a couple mg). There is also a list of random crystal – calcium oxolate crystal, brushite crystal, hydroxyapatite crystal, uric acid crystal, sodium urate crystal. These results showed up on my online patient account and said they were computer generated, and now since its the weekend I have to wait to until atleast monday to talk to the doctor. Mixed with how horrible i am already feeling, it is making my anxiety go through the roof. I would appreciate any feedback. Thank-you!!

      • Frederic L Coe

        Hi Katie, I guess the 24 hour urine results are indeed helpful. Your urine calcium is indeed high, and this may be in part from your very high sodium intake, but also your collection seems out of range. Urine creatinine arises from muscle, and most women do not have 2415 mg a day – usually about 1/2 of that. Perhaps this was a 48 hour collection? Even if I correct your urine calcium by dividing through by your creatinine, it is very high, about 200 mg calcium/gm urine creatinine, and so I suspect you have idiopathic hypercalciuria (your serum calcium was normal, 9.1). You do not give your urine volume, oxalate, or citrate, all important, so I cannot say much more. But I am sure the hypercalciuria can be easily corrected. Regards, Fred Coe

      • Jennifer Hochgesang

        Hi- I was just reading through this and am not a doctor, just a patient. The rash you describe sounds a lot like a butterfly rash of lupus. You may already know or have eliminated that as a possibility but just in case, I wanted to share. Hope things get better for you. Many blessings.

    • Frederic L Coe

      Hi Katie, without the 24 hour urines one cannot say or do much. Are you taking any medications? Some promote stones. Given the increasing pace, has anything changed in your life? The rash is not so obvious a clue, nor the white blood cell count. If you like, post the 24 hour urine results – I bet they help. Regards, Fred Coe

  8. Anne L. Danahy

    Why do I not see my comment posted? Did I miss something?

    Anne Danahy

  9. Anne L. Danahy

    Hi Dr. Coe,

    I just sent you a question about my calcium phosphate kidney stones.
    I said they were 7 cm. Correction,
    7 mm. Other than that, I saw after I sent it that my smart phone had done it’s own strange editing, but I think it is still decipherable.


    • Fredric Coe, MD

      Hi Anna, I am sorry to be a bit late; we have had some trouble with the comments reply pages this past week or so. I believe I answered you as best I can. Regards, Fred

  10. Concetta Spatola

    Hi Dr. Coe, I’am a 47 years old Woman, I’ve been having kidney stones for over 7 years, at least once a year I get them removed. The composition of the last stones removed was 98% of Calcium Phosphate. Any advice please.


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